Medullary thyroid cancer (MTC) is a rare tumor arising from the calcitonin-producing parafollicular C cells of the thyroid gland, occurring either sporadically or alternatively in a hereditary form based on germline RET mutations in approximately one-third of cases.
The aim of this study was to evaluate clinical findings, surgical therapy, and outcome for 56 patients affected by PHPT among 249 MEN-IIa patients collected from 84 families assembled by the Groupe d'Etude des Tumeurs á Calcitonine (GETC, French CalcitoninTumors Study Group).
Immunohistochemically, there were no significant correlations between the outcome of the patients and the expression of calcitonin (CT), carcinoembryonic antigen (CEA), calcitonin gene-related peptide (CGRP), or chromogranin A (CgA) in the primary tumors, and there were no differences in expression of these antigens between the primary and the recurrent tumors.
We analyzed their clinicopathologic factors, and cut-off values of tumor size and calcitonin levels were calculated using a receiver operating characteristic curve.
But immunohistochemical staining revealed vasoactive intestinal polypeptide and calcitonin only in a few cells, and it was still obscure what kinds of hormones were produced in this tumour.
The alternative RNA processing pathways in human calcitonin gene (CALC-I gene) expression were investigated using steady state RNA isolated from human medullary thyroid carcinoma (MTC) and from a culture line derived from this tumor.
There is a clear trend toward more positive scans with the higher calcitonin values, but patients with moderately elevated calcitonin values should also be taken into consideration for molecular imaging with F-DOPA PET/CT as the tumor burden in these patients is probably low, enabling further therapy to be individualized and consequently more efficient.
The proven power of DNA ploidy to predict mortality risk in medullary thyroid carcinoma (MTC) may be weakened when analyzed in conjunction with calcitonin immunoreactivity (CI) and amyloid staining (AS) of tumors.
In multivariate analysis, factors predicting biochemical cure and calcitonin level ≤500 pmol/L were no metastatic lymph nodes in the lateral neck (<i>p</i> = 0.030) and tumor diameter ≤20 mm (<i>p</i> < 0.001), respectively.
We subjected the promoter regions of two genes residing at 11p, namely the tumour-suppressor gene WT1 (Wilms' tumour gene) (11p13) and the calcitonin gene (11p15.5), to methylation analysis in human sporadic colorectal cancer using genomic sequencing.
The ectopic secretion of calcitonin (CT) by a wide variety of nonthyroidal human tumors has been studied by CT RIA, but little information is available concerning the biosynthesis of CT in these tumors.
Clinical data showed that 75% of the patients whose tumor carried ret mutation had tumor recurrence and/or increased serum calcitonin concentrations during the postsurgical follow-up period as opposed to 10% of the patients without mutations (P < 0.02, by chi2 analysis).
However, no evidence could be found for CGRP gene expression in tumour tissue from the same patients as judged by immunocytochemistry or in-situ hybridization using CGRP cRNA probes.
Sporadic cases had a higher median pre-op calcitonin (969.5 vs. 257.5 pg/ml), greater mean primary tumour size (23.5 vs. 12.5 mm) and more distant metastases (12.8 vs. 10.3%).
A positive correlation was found between the sonographically determined tumor mass (number/size of nodules/metastases) and the plasma calcitonin level.
Site-specific methylation changes, as revealed by the use of methylation-sensitive restriction enzymes, have been reported to occur in the promotor region of the calcitonin gene in chronic myeloid leukemia as it progresses from the chronic phase to blast crisis, in non-Hodgkin's lymphoid neoplasms and in non-lymphocytic leukemia.
WT CALCR, but not the mutant versions, inhibited Ras-mediated transformation of immortalized astrocytes <i>in vitro</i> Furthermore, calcitonin inhibited patient-derived neurosphere growth and <i>in vivo</i> glioma tumor growth in a mouse model.<b>Conclusions:</b> We demonstrate CT-CALCR signaling axis is an important tumor suppressor pathway in glioma and establish CALCR as a novel therapeutic target for GBM.<i></i>.
Medullary thyroid carcinoma (M.C.T.) is a tumour of the calcitonin-secreting cells of the thyroid gland; it affects both lobes, has a variable malignant potential, and is often familial.
In these patients, the timing and extent of surgery may depend not only on the patient's age and serum levels of the tumour marker calcitonin but also on the specific germline RET proto-oncogene mutation.
Prox1 also showed significant difference in expression according to chromogranin A and calcitonin immunohistochemical expression, with higher Prox1 expression in tumors with stronger chromogranin A or calcitonin staining.